Medicine 1 1

SHOCK
Dr. Hesham Kamal Habeeb Keryakos

Definition, pathophysiology, features and epidemiology of shock

Definition
 Shock is best defined as a life-threatening, generalized form of acute circulatory failure
associated with inade quate oxygen utilization by the cells.
 SHOCK IS THE CLINICAL EXPRESSION OF CIRCULATORY FAILURE THAT results in
inadequate cellular oxygen utilization. Shock is a common condi tion in critical care,
affecting about one third of patients in the intensive care.

 Q: Define Shock?
Acute clinical syndrome resulting from Inadequate oxygen delivery to meet the body
metabolic needs that results in Global tissue hypoperfusion and metabolic acidosis.

Oxygen Delivery to Tissues

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SHOCK IS A COMMON CONDITION IN CRITICAL CARE

 Q: Differentiate Hypotension From Shock?

 Always a symptom of primary cause
 Always hypoperfusion
– Hypotension, tachycardia, tachypnea
– Oliguria: urine output < 0.5 ml/kg BW/hour
– Altered mental status
– Metabolic acidosis, abnormal renal and liver function tests
 Usually, hypotension
– Shock with normal BP
– Low BP without hypoperfusion

How to identify patient in shock?

Diagnosis of shock is based on three components …
 Systemic arterial hypotension
BP below patient’s baseline, often defined as SBP <90 mmHg or MAP < 65 mmHg
 Clinical signs of tissue hypoperfusion

 Hyperlactatemia
> 1.5 mmol/L (normal blood lactate level is 1 mmol/L)

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 Do You Remember How To Quickly Estimate Blood Pressure By Pulse?

Pathophysiologic Mechanisms
 What are the five Types Of Shock?

 Dissociative (oxygen not appropriately bound or released from hemoglobin)

 Carbon monoxide poisoning
 Methemoglobinemia.

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SEPTIC SHOCK IS THE MOST COMMON FORM OF SHOCK

HYPOVOLEMIC SHOCK
 History: Fluid or Blood loss / External or Internal loss
– Skin (burn, exudative skin lesions)
– Respiratory (pleural effusion, bronchorrhea)
– GI loss (vomiting, diarrhea, gastrointestinal bleeding)
– Renal loss (diuretics, uncontrolled diabetes mellitus, diabetes insipidus)
– Third spacing (pancreatitis, crush injury, hypoalbuminemia)

 Findings
– Hypotension
– Altered mental state
– Diminished skin turgor
– Dry skin and mucosa
– Oliguria
– Low urine Na and high urine osmolarity
– BUN:Creat > 20:1

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OBSTRUCTIVE SHOCK

OBSTRUCTIVE SHOCK - CARDIAC TAMPONADE

Pericardiocentesis

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OBSTRUCTIVE SHOCK – TENSION PNEUMOPTHORAX

Tube Thoracostomy

OBSTRUCTIVE SHOCK – MASSIVE PULMONARY EMBOLISM

Thrombolytics

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CARDIAC TAMPONADE AND PULMONARY EMBOLISM

 Cardiac tamponade
Equalization of RAP, diastolic PA pressure, and PCWP
 Pulmonary embolism:
Elevated PAP with normal PCWP

CARDIOGENIC SHOCK

DISTRIBUTIVE SHOCK

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INITIAL APPROACH TO THE PATIENT IN SHOCK

 Early adequate resuscitation (VIP)
- Ventilate – oxygen administration
- Infuse – fluid resuscitation
- Pump – administration of vasoactive & inotropic agents
 Rapid correction of the cause
 If the condition is not rapidly reversed – insertion of
- Arterial catheter – monitoring of ABP and blood sampling
- Central venous catheter – infusion of fluids and vasoactive
agents + guide fluid therapy (CVP & ScvO2)

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EARLY TREATMENT – RESUSCITATION (ABCDE)

A - ESTABLISH THE AIRWAY
 Airway control is best achieved through endotracheal intubation.
 Determine need for intubation
1. severe dyspnea,
2. hypoxemia,
3. persistent or worsening acidemia (pH
<7.30)
 BUT: intubation can worsen hypotension
 Sedatives used to facilitate intubation may
cause arterial vasodilation, venodilation,
or myocardial suppression that may
result in hypotension.
 Positive pressure ventilation decreases preload and COP
Sedative agents + positive-pressure ventilation ➙ hemodynamic collapse.


 How to avoid hemodynamic collapse???

B - CONTROL THE WORK OF BREATHING

 Control of breathing is required when significant tachypnea accompanies shock?
 Respiratory muscles consume a significant amount of oxygen and contribute to
lactate production.
 Mechanical ventilation and sedation decrease work of breathing and improves
survival
 Neuromuscular blockers should be considered to decrease respiratory muscle
oxygen consumption.

C - OPTIMIZE THE CIRCULATION

 Two Large bore peripheral venous lines.
 Central venous access may aid in

 Assessing volume status (preload)

 Monitoring ScvO2.

The Trendelenburg position DOES NOT improve

cardiopulmonary performance compared with the
supine position?
 Passive leg raising above the level of the heart with the patient supine may be
effective. If passive leg raising results in an increase in blood pressure or CO, fluid
resuscitation is indicated.

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 OPTIMIZE THE CIRCULATION – IV FLUIDS
 MOST patients with shock have either an absolute or relative volume deficit, EXCEPT
patient in cardiogenic shock with pulmonary edema
 Fluid challenge: infusion of 300 to 500 ml of normal saline over 20 to 30 minutes, and
reassess the patient after each bolus.
 Isotonic crystalloids (normal saline or balanced crystalloids [lactated ringer or
plasmalyte]) are preferred over colloids (albumin or pentastarch).
- No outcome benefit from colloids
- Lactated Ringer or plasmalyte are preferred over normal saline?
 Titrated to:
- CVP 8-12 mm Hg
- Urine output 0.5 ml/kg/hr (30 ml/hr)
- Improving heart rate
 Positive fluid balance is harmful.

OPTIMIZE THE CIRCULATION - VASOPRESSORS

 When to use?
- inadequate response to volume resuscitation or
- contraindications to volume infusion.
 Most effective when the vascular space is “full”
 Patients with chronic hypertension may be at greater risk of renal injury at lower
blood pressures; however, in others, there appears to be no mortality benefit in
raising MAP > 65 to 70 mm Hg range.
 Although vasopressors improve perfusion pressure in the large vessels, they may
decrease capillary blood flow in certain tissue beds, especially the GI tract and
peripheral vasculature.
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 In addition to a vasopressor, an inotrope may be needed to directly increase CO by
increasing contractility and stroke volume
 Vasoactive agents:
- Norepinephrine is the first choice.
- Low-dose vasopressin in patients with septic shock
- Dobutamine If venous O2 saturation target not achieved (despite of achieving CVP
target)

D- ASSESS ADEQUATE OXYGEN DELIVERY

 ↓ oxygen consumption (VO2):
 Shock is associated with a hyperadrenergic state ➙ ↑ oxygen consumption is due to:
- Compensatory response to shock
- Anxiety Anxiolytics
- Pain Analgesics
- Shivering Avoid shivering

 ↑ Oxygen delivery (DO2)➙ Maintain arterial oxygen saturation/content

- Give supplemental oxygen
- Maintain Hemoglobin > 10 g/dL
↑COP using volume infusion or inotropic agents in incremental amounts
 Pulse oximetry is unreliable.
 Serial lactate levels or central venous oxygen saturations to assess tissue oxygen
extraction

E- ACHIEVE ENDPOINTS OF RESUSCITATION

 Goal of resuscitation is to maximize survival and minimize morbidity
 Use objective hemodynamic and physiologic values to guide therapy
 Goal directed approach
- MAP > 65 mm Hg
- Urine output > 0.5 mL/kg/hr
- CVP 8-12 mmHg
- Central venous oxygen concentration > 70%
 Consider Permissive hypotension (< 80 mmHg except with TBI) in hemorrhagic shock
(to avoid dilutional coagulopathy and increased bleeding)

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REMEMBER - TREATMENT OF THE CAUSE

Bleeding → Control of bleeding
Acute coronary syndromes → Percutaneous coronary intervention
Massive pulmonary embolism → Thrombolysis or embolectomy
Septic shock → Antibiotics and source control

SHOCK MANAGEMENT
 A “normal” blood pressure does not exclude the diagnosis of shock, and hypotension
may occur in the absence of shock
 Laboratory evidence for inadequate oxygenation:
- Serum lactate
- Multiorgan dysfunction
 EARLY RECOGNITION, EARLY RECOGNITION, EARLY RECOGNITION!
 EARLY RESUSCITATION, EARLY RESUSCITATION, EARLY RESUSCITATION!

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